Search results for "epithelium"

showing 10 items of 505 documents

Role of α1-adrenoceptor subtypes on corneal epithelial thickness and cell proliferation in mice

2018

Adrenergic stimuli are important for corneal epithelial structure and healing. The purpose of the present study was to examine the hypothesis that the lack of a single α1-adrenoceptor (α1-AR) subtype affects corneal epithelial thickness and cell proliferation. Expression levels of α1-AR mRNA were determined in mouse cornea using real-time PCR. In mice devoid of one of the three α1-AR subtypes (α1A-AR−/−, α1B-AR−/−, α1D-AR−/−) and in wild-type controls, thickness of individual corneal layers, the number of epithelial cell layers, and average epithelial cell size were determined in cryosections. Endothelial cell density and morphology were calculated in corneal explants, and epithelial cell p…

0301 basic medicinePhysiologyChemistryCell growthAdrenergicCell Biologyα1 adrenoceptorCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structure030221 ophthalmology & optometrymedicineα adrenoceptorsCorneal epitheliumAmerican Journal of Physiology-Cell Physiology
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Interactions between odorants and glutathione transferases in the human olfactory cleft

2020

AbstractXenobiotic metabolizing enzymes and other proteins, including odorant-binding proteins located in the nasal epithelium and mucus, participate in a series of processes modulating the concentration of odorants in the environment of olfactory receptors (ORs) and finely impact odor perception. These enzymes and transporters are thought to participate in odorant degradation or transport. Odorant biotransformation results in 1) changes in the odorant quantity up to their clearance and the termination of signaling and 2) the formation of new odorant stimuli (metabolites). Enzymes, such as cytochrome P450 and glutathione transferases (GSTs), have been proposed to participate in odorant clea…

0301 basic medicinePhysiologyOlfaction03 medical and health sciencesBehavioral NeuroscienceGSTP1chemistry.chemical_compound0302 clinical medicineOlfactory MucosaPhysiology (medical)glutathione transferasemedicine[SDV.MHEP.PHY]Life Sciences [q-bio]/Human health and pathology/Tissues and Organs [q-bio.TO]HumanshumanReceptorGSTP1odorantchemistry.chemical_classificationbiologymusculoskeletal neural and ocular physiology[SCCO.NEUR]Cognitive science/NeuroscienceCytochrome P450TransporterGlutathioneSensory Systems3. Good health030104 developmental biologymedicine.anatomical_structureEnzymeGSTA1chemistryBiochemistryOdorantsbiology.proteinOlfactory epithelium[SDV.AEN]Life Sciences [q-bio]/Food and Nutrition030217 neurology & neurosurgerypsychological phenomena and processesolfaction
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Protease‐activated receptor signaling in intestinal permeability regulation

2019

Protease-activated receptors (PARs) are a unique class of G-protein-coupled transmembrane receptors, which revolutionized the perception of proteases from degradative enzymes to context-specific signaling factors. Although PARs are traditionally known to affect several vascular responses, recent investigations have started to pinpoint the functional role of PAR signaling in the gastrointestinal (GI) tract. This organ is exposed to the highest number of proteases, either from the gut lumen or from the mucosa. Luminal proteases include the host's digestive enzymes and the proteases released by the commensal microbiota, while mucosal proteases entail extravascular clotting factors and the enzy…

0301 basic medicineProteasesCell typeProtease-activated receptorReceptors Proteinase-ActivatedBiologyBiochemistryPermeabilityEpitheliumInflammatory bowel disease03 medical and health sciencesGastrointestinal cancer0302 clinical medicineImmune systemmedicineAnimalsHumansProtease-activated receptorIntestinal MucosaSymbiosisReceptorMolecular BiologyMicrobial proteasesGastrointestinal NeoplasmsClotting factorIntestinal permeabilityCoagulationMicrobiotaEpithelial barrier functionCell BiologyInflammatory Bowel Diseasesmedicine.diseaseIntestinal epitheliumTissue factorGastrointestinal MicrobiomeCell biologyIntestineGastrointestinal TractDisease Models Animal030104 developmental biologyGene Expression RegulationBacterial Translocation030220 oncology & carcinogenesisPeptide HydrolasesSignal Transduction
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Influenza virus damages the alveolar barrier by disrupting epithelial cell tight junctions

2016

A major cause of respiratory failure during influenza A virus (IAV) infection is damage to the epithelial–endothelial barrier of the pulmonary alveolus. Damage to this barrier results in flooding of the alveolar lumen with proteinaceous oedema fluid, erythrocytes and inflammatory cells. To date, the exact roles of pulmonary epithelial and endothelial cells in this process remain unclear.Here, we used an in vitro co-culture model to understand how IAV damages the pulmonary epithelial–endothelial barrier. Human epithelial cells were seeded on the upper half of a transwell membrane while human endothelial cells were seeded on the lower half. These cells were then grown in co-culture and IAV wa…

0301 basic medicinePulmonary and Respiratory Medicine030106 microbiologyBiologymedicine.disease_causeVirusCell LineTight Junctions03 medical and health sciencesInfluenza A Virus H1N1 SubtypemedicineInfluenza A virusHumansTight junctionInfluenza A Virus H5N1 SubtypeEpithelial CellsVirologyIn vitroEpitheliumCoculture TechniquesCell biologyPulmonary Alveoli030104 developmental biologymedicine.anatomical_structureCell cultureCytokinesPulmonary alveolusLumen (unit)European Respiratory Journal
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Functional characterization of a novel 3D model of the epithelial-mesenchymal trophic unit

2017

Background/Aim: Epithelial-mesenchymal communication plays a key role in tissue homeostasis and abnormal signaling contributes to chronic airways disease such as COPD. Most in vitro models are limited in complexity and poorly represent this epithelial-mesenchymal trophic unit. We postulated that cellular outgrowth from bronchial tissue would enable development of a mucosal structure that recapitulates better in vivo tissue architecture. Materials and Methods: Bronchial tissue was embedded in Matrigel and outgrowth cultures monitored using time-lapse microscopy, electrical resistance, light and electron microscopy. Cultures were challenged repetitively with cigarette smoke extract (CSE). Res…

0301 basic medicinePulmonary and Respiratory MedicinePathologymedicine.medical_specialtyClinical BiochemistryBronchiRespiratory MucosaBiologyImmunofluorescenceModels Biologicalfibroblastbronchial03 medical and health sciencesIn vivoSmokemedicineHumansFibroblastMolecular BiologyCells CulturedTissue homeostasisMicroscopyMatrigelECMelectron microscopymedicine.diagnostic_testcigarette smokeMesenchymal stem cellEpithelial CellsMesenchymal Stem CellsEpitheliumCell biologyDrug Combinations030104 developmental biologymedicine.anatomical_structurein vitro modelMotile ciliumProteoglycansCollagenLamininepitheliumExperimental Lung Research
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Meta-analysis of gene-environment-wide association scans accounting for education level identifies additional loci for refractive error

2016

Myopia is the most common human eye disorder and it results from complex genetic and environmental causes. The rapidly increasing prevalence of myopia poses a major public health challenge. Here, the CREAM consortium performs a joint meta-analysis to test single-nucleotide polymorphism (SNP) main effects and SNP × education interaction effects on refractive error in 40,036 adults from 25 studies of European ancestry and 10,315 adults from 9 studies of Asian ancestry. In European ancestry individuals, we identify six novel loci (FAM150B-ACP1, LINC00340, FBN1, DIS3L-MAP2K1, ARID2-SNAT1 and SLC14A2) associated with refractive error. In Asian populations, three genome-wide significant loci AREG…

0301 basic medicineRefractive errorgenetic structuresGeneral Physics and AstronomyGenome-wide association studyVARIANTSrefractive error ; geneEYEBioinformaticsINCIDENT MYOPIAGenome-wide association studiesSensory disorders Donders Center for Medical Neuroscience [Radboudumc 12]0302 clinical medicinePolymorphism (computer science)10. No inequalityPOPULATIONeducation.field_of_studyMultidisciplinaryQACTIVATED PROTEIN-KINASEta3142single-nucleotide polymorphismRETINAL-PIGMENT EPITHELIUMOUTDOOR ACTIVITY3142 Public health care science environmental and occupational health3. Good healthRefractive errorsMeta-analysislociEducational StatusSciencePopulation610 Medicine & healthEnvironmentBiologyta3111Polymorphism Single NucleotideArticleWhite PeopleGeneral Biochemistry Genetics and Molecular BiologyEducation03 medical and health sciencesAsian PeopleSDG 3 - Good Health and Well-beingGenetic variationmedicineHumansSNPGenetic Predisposition to Diseasemyopia3125 Otorhinolaryngology ophthalmologyGenetic variationeducationRECEPTORGene Expression Profilingta1184General ChemistryHeritabilitymedicine.diseaseeye diseasesta3125TIME OUTDOORS030104 developmental biologyGenetic LociEvolutionary biologyRISK-FACTORS030221 ophthalmology & optometryREsense organs3111 BiomedicineGenome-Wide Association StudyNature Communications
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Subacute effects of ozone exposure on cultivated human respiratory mucosa.

2001

This study was designed to investigate subacute effects of long-term exposure of both healthy and chronically inflamed human respiratory mucosa to ozone. Functional and metabolic effects on ciliary beat frequency (CBF), release of interleukin 8 (IL-8), interleukin 4 (IL-4), and γ interferon (g-INF), as well as cellular viability and cytotoxicity, were monitored. Cell cultures of 60 specimens (healthy mucosa: n = 30, inflamed mucosa: n = 30) were exposed to synthetic air and to ozone-enriched synthetic air in different concentrations of WO, 500, and WOO μg/m3. Continuous expositions were performed using an air/liquid interface cell culture technique for a period of 4 weeks. CBF was monitore…

0301 basic medicineRespiratory MucosaAdultmedicine.medical_specialtyTime FactorsAdolescentMucociliary clearanceCell Survivalmedicine.medical_treatmentRespiratory Mucosa03 medical and health scienceschemistry.chemical_compoundInterferon-gamma0302 clinical medicineOzoneLactate dehydrogenaseInternal medicinemedicineHumansInterleukin 8CiliaCytotoxicityInterleukin 4Cells CulturedAged030102 biochemistry & molecular biologybusiness.industryAirInterleukin-8Middle AgedCytokineEndocrinologyOtorhinolaryngologychemistry030220 oncology & carcinogenesisAnesthesiaRespiratory epitheliumInterleukin-4businessAmerican journal of rhinology
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N-retinylidene-N-retinylethanolamine adduct induces expression of chronic inflammation cytokines in retinal pigment epithelium cells

2021

Blindness due to photoreceptor degeneration is observed in both genetic and acquired eye disorders. Long blue light exposure can contribute to increase levels of oxidative compounds within the retinal pigment epithelium (RPE), enhancing risk of retinal damage. In retina, reactive oxygen species contribute to the activation of inflammatory cascade. If chronic, this inflammatory response can result in photoreceptor death. Therefore, we investigated the effects of the endogenous adduct N-retinylidene-N-retinylethanolamine (A2E) on RPE cells, in order to identify the most dysregulated cytokines and their related inflammatory pathways. RPE cells were exposed to A2E and blue light for 3h and 6h. …

0301 basic medicineRetinal degenerationCell SurvivalInflammationRetinal Pigment Epitheliummedicine.disease_causeA2ECell LineTranscriptomeRetinoids03 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineExpression analysiSettore BIO/13 - Biologia ApplicatamedicineHumansInflammationchemistry.chemical_classificationRetinaReactive oxygen speciesRetinal pigment epitheliumSettore MED/30 - Malattie Apparato VisivoChemistryRetinal Degenerationmedicine.diseaseeye diseasesSensory SystemsCell biologyOphthalmology030104 developmental biologymedicine.anatomical_structureGene Expression RegulationChronic Disease030221 ophthalmology & optometryOxidative streCytokinesEye disorderRPEA2E; Expression analysis; Inflammation; Oxidative stress; RPE; Retinal degenerationsense organsmedicine.symptomReactive Oxygen SpeciesRetinal PigmentsOxidative stressSignal TransductionExperimental Eye Research
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Primary Cilium-Mediated Retinal Pigment Epithelium Maturation Is Disrupted in Ciliopathy Patient Cells

2018

SUMMARY Primary cilia are sensory organelles that protrude from the cell membrane. Defects in the primary cilium cause ciliopathy disorders, with retinal degeneration as a prominent phenotype. Here, we demonstrate that the retinal pigment epithelium (RPE), essential for photoreceptor development and function, requires a functional primary cilium for complete maturation and that RPE maturation defects in ciliopathies precede photoreceptor degeneration. Pharmacologically enhanced ciliogenesis in wild-type induced pluripotent stem cells (iPSC)-RPE leads to fully mature and functional cells. In contrast, ciliopathy patient-derived iPSC-RPE and iPSC-RPE with a knockdown of ciliary-trafficking pr…

0301 basic medicineRetinal degenerationInduced Pluripotent Stem CellsRespiratory MucosaRetinal Pigment EpitheliumBiologyCell MaturationCiliopathiesArticleGeneral Biochemistry Genetics and Molecular BiologyMice03 medical and health sciencesCiliogenesismedicineAnimalsCiliaInduced pluripotent stem celllcsh:QH301-705.5Mice KnockoutRetinal pigment epitheliumCiliumRetinal Degenerationmedicine.diseaseCiliopathieseye diseasesCell biologyProtein Kinase C-deltaCiliopathy030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)sense organsCell Reports
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Generation of an inducible RPE-specific Cre transgenic-mouse line.

2018

The retinal pigment epithelium (RPE) is an epithelial monolayer in the back of the vertebrate eye. RPE dysfunction is associated with retinal degeneration and blindness. In order to fully understand how dysregulation affects visual function, RPE-specific gene knockouts are indispensable. Since the currently available RPE-specific Cre recombinases show lack of specificity or poor recombination, we sought to generate an alternative. We generated a tamoxifen-inducible RPE-specific Cre transgenic mouse line under transcriptional control of an RPE-specific Tyrosinase enhancer. We characterized the Cre-mediated recombinant expression by crossing our RPE-Tyrosinase-CreErT2 mouse line with the tdTo…

0301 basic medicineRetinal degenerationMaleEmbryologylcsh:MedicineGene ExpressionRetinal Pigment EpitheliumBiochemistry0302 clinical medicineRecombinaseMedicine and Health Scienceslcsh:ScienceStainingMultidisciplinaryMonophenol MonooxygenaseAnimal ModelsSpecimen preparation and treatmentCell biologyEnzymesmedicine.anatomical_structureExperimental Organism SystemsModels AnimalFemaleAnatomyResearch ArticleGenetically modified mouseImaging TechniquesTransgeneOcular AnatomyMice TransgenicMouse ModelsBiologyResearch and Analysis MethodsRetinaRecombinases03 medical and health sciencesModel OrganismsOcular SystemFluorescence ImagingmedicineGeneticsAnimalsEnhancerGene knockoutRetinaRetinal pigment epitheliumIntegraseslcsh:REmbryosDAPI stainingBiology and Life SciencesProteinsmedicine.diseaseeye diseasesMice Inbred C57BLLuminescent Proteins030104 developmental biologyNuclear stainingEnzymologyAnimal StudiesEyeslcsh:Qsense organsHead030217 neurology & neurosurgeryDevelopmental BiologyPloS one
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